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The inflammatory response of RA causes autophagy in FLSs to produce putrescine, which intensifies inflammation of GABA and H2O2 through the MAO-B in the joint. In chronic inflammation, increased IL-1β passes through a loose blood-brain barrier and enters the brain. Increased IL-1β in the hippocampus causes cognitive impairment by activating astrocytes and by inhibiting synapse signaling by increasing the secretion of the inhibitory neurotransmitter GABA from MAO-B. Furthermore, the use of an MAO-B inhibitor can suppress the MAO-B of FLSs and astrocytes to relieve inflammation of the joints and alleviate cognitive function.
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